Venous diseases

Division of Vascular Surgery

Department of Surgery

Addis Ababa University SOM

 Objectives

 Sx , Sn and complications of VD(venous disorders)

 diagnostic workup of VD

 Differentiate the various causes of leg ulcers

 Evaluate adv. & disadv Management modalities in VVs

Risk factors & diagnosis of DVT

 Prevention , Mgt & complications of DVT

 Anatomy of venous systems

communicating
Intersaphenous vein
(Vein of Giacomini)

perforators
Paratibial perforator
Great saphenous vein
Perforator or femoral Deep veins
(GSV)
canal Common femoral vein
Small saphenous vein
(Superficial) femoral vein (SSV)
Deep femoral vein
 Vein Anatomy

Great
Great

Small
Small
 New Nomenclature of the lower extremity veins

Old Terminology New Terminology

Greater or long saphenous vein
Lesser or short saphenous vein
Common femoral vein
Superficial femoral vein
Giacomini vein
Hunter’s perforators
Dodd’s perforators
Boyd’s perforators
Sherman’s(‘24cm’) perforators
Cockett’s perforator (I, II, III)
Great saphenous vein (GSV)
Small saphenous vein (SSV)
Common femoral vein
Femoral vein
Intersaphenous vein
Mid thigh perforators
Perforators of the femoral canal
Paratibial perforator (proximal)
Paratibial perforator
Posterior tibial perforators (lower, middle, upper)

An international interdisciplinary consensus statement (Caggiati et al. J Vasc Surg 2002;36:416)

 Differential diagnosis of leg ulcers
• Venous stasis ulcer
; chronic venous insufficiency
• Ischemic ulcer
; arterial insufficiency (ASO,
Buerger’s disease)
• Neurotrophic ulcer
; DM foot, neuropathy
A typical leg affected by CVI will be edematous, with
edema increasing over the course of the day. The leg may
also be indurated and pigmented with eczema and
dermatitis. These changes are associated with excessive
proteinaceous capillary exudate and deposition of a
pericapillary fibrin cuff that may limit nutritional
exchange. In addition, an increase in white blood cell
trapping within the skin microcirculation in CVI patients
may lead to microvascular congestion and thrombosis.
Subsequently, white blood cells may migrate into the
interstitium and release necrotizing lysosomal enzymes,
potentially leading to tissue destruction and eventual
ulceration.
 Venous stasis ulcer

• Location

; distally, above medial malleolus

• Skin around ulcer

; pigmented, fibrotic

• Pain

; not severe, relieved by elevation

• Associated gangrene ; absent

• Bleeding from ulcer ; venous ooze

• Associated signs

; edema, pigmentation,

dependent cyanosis
 Ischemic ulcer

• Location

; toes, lateral malleolus

pressure point

• Skin around ulcer ; shiny, atrophic

• Pain ; severe, relieved by dependency

• Associated gangrene ; may be present

• Bleeding from ulcer ; little or none

• Associated signs

; decreased pulse, pallor on elevation,

dependent rubor
 Neurotrophic ulcer

• Location
; pressure point,
areas of decreased sensation
• Demonstrable neuropathy
• Skin around ulcer ; callused
• Pain ; none, ulcer may go unnoticed
• Associated gangrene ; absent
• Bleeding from ulcer ; brick red
• Associated signs
; decreased sensation,
absent ankle reflexes
 Dry gangrene Wet gangrene

• Hard • Soft Edematous

• Withered • Foul-smelling drainage
• No infectious component • Infectious cause
• Dry gangrene is characterized by its hard, dry texture, usually occurring in the distal aspects of toes
and fingers, often with a clear demarcation between viable and necrotic tissue. This form of gangrene
is more common in patients with atherosclerotic disease and frequently results from embolization to
the toe or forefoot. The patient may often give a history of associated claudication or foot and toe pain.
– Once demarcation has occurred, the involved digit may be allowed to autoamputate without further proximal
progression of gangrene. However, this is often a process which is both lengthy and disturbing to the patient.
On the other hand, many patients with dry gangrene do not have adequate circulation to heal a distal
amputation. As a result, most patients should be evaluated with angiography for possible distal bypass in
order to improve chances of healing a distal amputation and obtaining limb salvage.
• Wet gangrene is characterized by its moist appearance, gross swelling, and frequent blistering. It is a
true emergency, often occurring in diabetics with decreased sensation who sustain an unrecognized
trauma to the toe or foot. If sufficient viable tissue is present to maintain a functional foot, emergent
debridement of all affected tissue often results in healing. If the wet gangrene involves an extensive
portion of the foot, emergent guillotine amputation may be warranted, with revision to below knee or
above knee amputation 72 hours later
 Venous valve

• Bicuspid valves to prevent reflux

Turbulence in valve cusp

 Calf muscle pump ; “Peripheral Heart”

Venous sinuses of calf muscles

(calf muscle pump)

① Popliteal artery
② Popliteal vein
③ Small saphenous vein
④ Gastrocnemial veins
⑤ Soleal vein
⑥ Anterior tibial vein
⑦ Peroneal vein
⑧ Posterior tibial vein
 Venous disorders
• Venous insufficiency
– Chronic venous disorder (CVD)
• Chronic venous insufficiency (CVI)
– Varicose vein (VV)

• Venous thromboembolism (VTE)

– Superficial thrombophlebitis
– Deep vein thrombosis (DVT) / Pulmonary embolism (PE)
– Visceral venous thrombosis
• Portal vein thrombosis
• Mesenteric vein thrombosis
 Definitions
• Varicose vein
– Abnormally dilated saccular or cylindrical superficial veins, which can be
circumscribed or segmental (WHO)
• Venous insufficiency
– Any abnormality of the peripheral venous system that reduces or impedes
venous return.
• Chronic venous disorder (CVD: C1-C6)
– Full spectrum of morphological and functional abnormalities of the venous
system (telangiectasia – venous ulcer)
• Chronic venous insufficiency (CVI: C3-C6)
– Functional abnormality of the venous system and is usually reserved for
patients with more advanced disease including edema(C3), skin change(C4),
or venous ulcers (C5-C6)
• Patients complain of leg fatigue, discomfort, and heaviness. Signs of CVI may
include varicose veins, pigmentation, lipodermatosclerosis, and venous ulceration.
• CVI can be primary or secondary. Primary CVI results from intrinsic abnormalities
of the vein wall, whereas secondary CVI, so-called postthrombotic syndrome
(PTS), occurs as a result of DVT. The signs and symptoms of CVI can be therefore
be attributed to venous reflux, venous obstruction, calf muscle pump dysfunction,
or a combination of these factors, as well as loss of venous wall elasticity.
• In the majority of patients with CVI, the most important factor appears to be
venous reflux.
• Secondary valvular reflux is diagnosed when an identifiable cause is present. The
most frequent secondary cause is DVT.
 Pathogenesis of chronic venous insufficiency

• Vein wall defects in strength and characteristics

– collagen ↑, elastin ↓
• Anatomic and hemodynamic differences
– Main saphenous trunk ↓ vs. tributaries ↑
• Incompetence of venous valve
– Axial vein reflux
– Perforating vein reflux
• Venous hypertension
– Hydrostatic pressure : incompetent proximal (axial) valve
– Hydrodynamic pressure : failure of perforating vein
– Extravasation of macromolecule: fibrinogen, α-macroglobulin,
RBCs
– Edema, pigmentation, stasis dermatitis, lipodermatosclerosis
– Venous stasis ulcer
 Symptoms of CVI
Persistent venous hypertension
 capillary hyperpermeability
 escape of proteinaceous fluid and RBC
 hemosiderin deposition  hyperpigmentation
 Subcutaneous organization & fibrosis  Lipodermatosclerosis
 Acute or chronic inflammation
 Release of inflammatory mediators (cytokines)
 dry, scaly patches or plaques  stasis dermatitis
 Venous stasis ulcer
A typical leg affected by CVI will be
edematous, with edema increasing over the
course of the day. The leg may also be
indurated and pigmented with eczema and
dermatitis. These changes are associated
with excessive proteinaceous capillary
exudate and deposition of a pericapillary
fibrin cuff that may limit nutritional
exchange. In addition, an increase in white
blood cell trapping within the skin
microcirculation in CVI patients may lead
to microvascular congestion and
thrombosis. Subsequently, white blood cells
may migrate into the interstitium and
release necrotizing lysosomal enzymes,
potentially leading to tissue destruction and
eventual ulceration.
 CEAP classification
C (Clinical), E (Etiology), A (Anatomic), P (Pathophysiologoic)

C1

C2

C3
Chronic venous insufficiency (CVI, C3-C6: 만성 정맥부
전) C5
C4 C6
 CEAP classification
C(Clinical), E(Etiologic), A(Anatomic), P(Pathophysiologic)
 Varicose veins

• Incidence
– Over the age 40 -- 50% some form of varicosity or telangiectasia
– 10-20% significant VVs
– 0.5% VVs with chronic venous stasis and ulceration
• Risk factors
– Family history of VVs
– Age ; 50 years or over
– Female sex
– Multiparity ; 2 or more pregnancies
– Oral contraceptive use: affect viscosity of blood
– Standing vocation ; more than 6 hours/day
– Obesity
 Pathophysiology of primary VV

• Valvular incompetence
• Incompetence of perforating veins
• Arteriovenous communication
• Defect in structure of vein wall

• Congenital vascular malformation

– Klippel-Trenaunay syndrome
; limb hypertrophy, VVs, capillary port-wine stains
– Parkes-Weber syndrome
; limb hypertrophy, VVs, AV malformations
 Saphenous vein reflux
GSV insufficiency SSV insufficiency
(Great Saphenous Vein) (Small Saphenous Vein)
 Clinical finding of VV

• Signs and Symptoms

– Cosmetic appearance of the dilated tortuous veins
– Pain, fatigue, aching heaviness; dull, burning pain, gradual onset,
exacerbated by prolonged standing, often relieved by leg elevation
– Signs of CVI ; swelling, pigmentation, venous ulceration
– Itching,

• Differential diagnosis
– Arterial insufficiency
– AV malformation
– Congenital venous malformation
 Diagnosis of VV

• P/E
– In standing position
– Trendelenberg test, Perthes test
• Plethysmography
– Venous refilling time (VRT), Venous filling index (VFI)
Residual volume fraction (RVF), Ejection fraction (EF)
• Continuous hand-held doppler
– Presence of reflux
• Phlebography ; abandoned method
• Duplex USG
– Gold standard method
• CT venography ; New adjunctive method
VV. examination
Diagnosis: CT Venography

Rt GSV

Navigator in varicose vein surgery

Min SK et al. Journal of Vascular Surgery, 2010
Non-operative treatment of CVD

• Aim
– To improve valvular dysfunction
– To improve calf muscle pump action
• Leg elevation (toe above the nose)
• External compression (stocking)
– Gradual compression stocking
• 20-30 mmHg, daytime
– Caution to concomitant arterial insufficiency
• Local wound care to venous ulcer
- Unna boot : triple layer calamine, zinc oxide compressive dressing
• Intermittent pneumatic compression
Algorithm of varicose vein treatment

Cryo
 Treatment of C1 lesion
C1 26 gauge needle
Sclerotherapy
1. Intravenous injection of sclerosing venulectasia
agents
Intima destruction telangiectasia

Coagulum formation
reticular vein
Permanent fibrosis
Lumen obstruction

Repeat sessions: 2-6 times

(interval: 2 wks - 3 mo.)

+
2. Compressive therapy

• Initial point compression: 24-72 hr (<1mm), 3-5 days (1-3mm)

• Elastic stocking for 4–8 weeks
 Treatment Modalities of Saphenous Vein Incompetence
Axial vein control

Cryo
• High ligation and stripping
– Classic method
– Cryostripping

• Endovenous ablation
– Chemical ablation
• Ultrasound-guided sclerotherapy
• Transcatheter-guided sclerotherapy

– Thermal ablation
• Radiofrequency Ablation (RFA)
• Endovenous Laser Treatment (EVLT)

No prospective randomized trial to compare three modalities

(High ligation and stripping vs. RFA vs. EVLT)
 Principles for Varicose Vein Surgery
• No reflux, No varicose !

 Elimination of reflux

• Ablation of ugly tortuous vein

• Better functional & cosmetic result

• Op indication
– Venous ulcer

– Hyperpigmentation, lipodermatosclerosis

– External bleeding

– Superficial thrombophlebitis

– Leg heaviness, easy leg fatigue, aching pain, night cramps

– Cosmetic

– Pain unrelieved despite compression therapy

 Components of VV surgery

• High ligation
; Sapheno-femoral junction / sapheno-popliteal junction

• Stripping

• Perforator ligation

• Varicosectomy
– Stab avulsion
– Ambulatory phlebectomy: Excision and avulsion of superficial varicosities (ie,
phlebectomy) through multiple tiny incisions is referred to as “ambulatory
phlebectomy” or “micro-stab avulsion phlebectomy.”
 High ligation

S-F junction Standard transfixion

GSV
CFV

Flush HL

GSV

CFV
 Stripping ( 발거술 )

Conventional stripping Inversion stripping

( 이유 ) high recurrence after HL only.

( 방법 ) Stripping down to knee level,
not to ankle level
 Varicosectomy, phlebectomy

Ambulatory Phlebectomy (AP)

• Stab avulsion
Müller or Varady’s hook

Local anesthesia
No skin suture
No ligature
No narcosis
No immobilization
 Techniques
Vein access & Tip positioning (Knee puncture)
400-600μm laser
fiber

- Duplex-guided

- 1-2cm below the SFJ, SPJ

 Techniques
Perisaphenous tumescent anesthesia
250ml saline
60ml 1% lidocaine
with epinephrine(1:100,000)
6ml 8.4% sodium bicarbonate

1. Anesthesia
2. Vein contraction
3. Decrease in Cx.
10mm separation (phlebitis, burn)
(skin-GSV, around GSV)
 Techniques
Pullback treatment with Laser firing (810, 940, 980 nm diode laser)

Groin to knee
12-14 W Continuous mode (3000-3500 J)
Pullback speed: 1.5-2 mm/sec

Below knee
Optional
10 W pulsing (1sec) mode 1000-1500 J
Quick withdrawal
Subcutaneous tumescence
 Surgery for severe chronic venous insufficiency (C4-6)
1) Compression therapy: 15-57% with recurrence and disability
– Gradient elastic stocking, Intermittent pneumatic compression
– Unna boot, Circ-Aid
– Wound care
2) Superficial reflux ablation
– 16.8-50% of venous ulcer confined to superficial v. system, normal deep v. function
– Superficial reflux surgery + compression > compression only
– Surgery, EVLT, RFA
3) Perforating vein interruption
– Linton’s operation: problem of wound healing complication
– SEPS (Subfascial endoscopic perforator surgery):
• Single open scope procedure
• Laparoscopic instrument procedure (two port)
– Ultrasound-guided sclerotherapy
4) Direct venous reconstruction
– Femorofemoral crossover bypass (Palma)
– Direct valvuloplasty (Kistner), vein segment transfer (Kistner)
– External valvular reconstruction
Venous Thrombo-Embolic Disease (VTE)
 Venous Thromboembolic disease

• Deep Vein thrombosis / Pulmonary embolism

– Traveler’s thrombosis (Economy class syndrome)

• Other forms of venous thrombosis

– Superficial thrombophlebitis

– Axillary-Subclavian thrombosis

– Mesenteric venous thrombosis

 DVT
• It is an acute thrombosis of the deep veins.
The thrombus may commence in the venous tributary of a main
vein. The calf vein is the most frequent site of thrombosis.
- Pulmonary embolism occurs in 5 to 20 percent cases of calf
deep vein thrombosis.
 Clinical manifestation of DVT

• Mostly asymptomatic

• Pain, Edema

; due to vein obstruction,

inflammation of perivascular tissue,

lymphatic obstruction

• Distention of superficial veins

• Cutaneous erythema

• Homan’s sign

; calf pain with forced dorsiflexion of foot

Lymphedema
 Venous edema vs. Lymphedema

Venous edema Lymphedema

1. Pigmentation(+) 1. Edema on the dorsum of foot
2. Ulcer(+) 2. Minimal effect of leg elevation
3. Pain relief after leg elevation 3. Prior history of pelvic surgery
4. flariasis
Lipedema
Etiology of DVT
Fibrinolysis

Thrombosis

Of these risk factors, relative hypercoagulability appears most

important in most cases of spontaneous VTE, or so-called
idiopathic VTE, whereas stasis and endothelial damage likely play
a greater role in secondary VTE, or so-called provoked VTE,
occurring in association with transient risk factors such as
immobilization, surgical procedures, and trauma. Identifiable risk
factors for VTE generally relate to one of the conditions described
by Virchow.
 Risk factors for DVT

Liapise et al, European Manual of Medicine: Vascular Surgery

 Diagnosis of DVT

• D-dimer ; cross-linked degradation product of fibrin. [screening]

– High negative predictive value; 97-99%

– Absence rule out DVT

• Duplex USG ; test of choice [gold standard]

– Both anatomical and functional informations can be obtained by this single test. Filling

defects in flow and lack of compressibility indicate the presence of a thrombosis

• CT venography ; pelvic vein evaluation, PE study

• Impedence phlethysmography

• Ascending venography

• MR Venography

• Lung ventilation & perfusion scan

 Workups for DVT
• Before anticoagulation, Check coagulation profiles !

– CBC ; Hb, Hct, platelet A thrombophilic state leading to venous thrombosis

– BT / PT(INR) / aPTT
– AT-III, protein C, protein S
– Coagulation factors VIII, IX, XI
can be inherited or acquired:
•Congenital/inherited (eg, factor V Leiden, protein C
deficiency)
•Acquired (eg, following orthopedic surgery,
antiphospholipid antibody)
•Associated with systemic disease (eg, malignancy)

– Fibrinogen, FDP, D-dimer, homocysteine

– Lupus anticoagulant, anticardiolipin Ab, antiphospholipid Ab

– Family study in hereditary or familiar tendency

• Factor V Leiden, Prothrombin gene mutation ; rare

Duplex USG for DVT
 Duplex criteria for DVT

• Negative for DVT

– Complete approximation of the vein wall during compression
– Complete color filling of the lumen without any defect

• Positive for DVT

– Partially compressible or noncompressible vein
– Echogenic material within the vein
– Filling defect on color imaging
– Absence of doppler signal

Mansour & Labropoulos: Vascular Diagnosis(2005)

 DVT prophylaxis

 Indications  Mechanical Prophylaxis

– Major abdominal surgery  Activation of calf pump mechanism
– Major orthopedic surgery
; Early walking
– Major trauma
; “Out of bed into a chair”  Do not !
– Prolonged immobility (>3d)
; Sequential compression devices

 Pharmacological prophylaxis
 Low-dose unfractionated Heparin (UFH)
Recombinant plasminogen activator:
used as anticoagulant ; 5,000 u sc injection q 8 ~ 12
hr
 Low molecular weight heparin (LMWH)

ACCP guideline. Chest 2008;133(6 Suppl);454S-545S.

 DVT Treatment Modalities
 Treatment of DVT ; Anticoagulation

• Absolute contraindication  Unfractionated Heparin (UFH)

– Serious active bleeding  5,000-20,000 units iv bolus
– Recent NS op
 1,000-2,000 u/hr ivs with infusion pump
– Malignant HT
 aPTT level check ; q 4-6 hrs
– ICH / SAH
 Target aPTT basal level ; 1.5 ~ 2.0 times

• Relative contraindication longer than normal

– Recent surgery
– GI bleeding  Low molecular weight heparin (LMWH)
– Hemorrhagic diathesis  LMWH 7,500 U SC q 12-24 hrs
– Recent stroke

 Warfarin
 Heparin 2_3 days overlap with warfarin
 Target PT level ; INR 2.0 ~ 3.0
Clinical spectrum of acute DVT

Anticoagulation therapy

Strategy of thrombus removal

 Strategy of thrombus removal

• Rationale for thrombus removal

– Pathophysiology of CVI ; ambulatory venous HT
= venous valvular incompetence + luminal obstruction
– Thrombus removal
 elimination of luminal obstruction
 preservation of valve function
 Post-thrombotic syndrome avoided

– Method
• Surgical venous thrombectomy
• Thrombolysis
• Percutaneous pharmaco-mechanical thrombectomy
Treatment algorithm for iliofemoral
DVT

Comerota & Paolini. EJVES 2007;33:351-60

 IVC filter

 Changing trends in filter placement

• Increasing placement of IVC filters for prophylaxis

• Temporary, retrievable filter (vs. permanent)
• USG-guided bedside procedure (vs. Fluoroscopy-guided)

Ernst & Stanley. Current therapy in vascular surgery

 Questions ?

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